Early heart failure and hypoxia due to congenital heart disease frequently result in small children with sparse body fat. Although palliative surgery frequently provides symptomatic improvement, postoperative weight gain remains slow. On the other hand, surgical repair, especially if performed early, is often followed by improved weight gain with increased adipose tissue. Human and animal research have shown that adipose tissue growth in infancy is primarily due to a rapid increase in cell number. Thereafter, in normal rodents the rate at which cell number increases falls and tissue enlargement is produced mainly by increased cell size. In animals, nutritional deficiency during the early period of cell division can lead to permanent hypocellularity irrespective of subsequent correction. Therefore, we have postulated that young patients underweight with heart failure and/or hypoxia will have subnormal numbers of fat cells unless surgically improved during early life. Our data suggest that adipose hypocellularity is present in children with cyanotic congenital heart disease and early hypoxia, and in children with acyanotic congenital heart disease with early heart failure, supporting our hypothesis. In testing this hypothesis, a) total fat cell number, b) cell size and, c) cell function as well as, d) adipose tissue thymidine kinase and lipoprotein lipase activity are determined by methods employing small adipose tissue specimens obtained at cardiac catheterization and surgery. Patients are studied serially over several years. The cardiac patients are compared to patients without heart or metabolic disorders. With this information, the importance of hypoxia, heart failure, and palliative and reparative surgery in respect to age will be evaluated.